The skin is susceptible of various forms of stress such as ultraviolet light, heat, and chemical substances which exist in the environment because it is situated in the outer most surface of the human body. Among other forms of stress mentioned above, the ultraviolet light (particularly the UVB having a wavelength region of 290-320 nm) is reputed to generate active oxygen and free radicals on the skin surface and in the cutaneous tissues and form the cause for sunburn and cutaneous cancer (“Active Oxygen and Morbidity” compiled and written by Masayasu Inoue and published by by Gakkai Shuppan Centeron Oct. 1, 1992, pp.567-576). Particularly, since the amount of the ultraviolet light that reaches the surface of the earth in consequence of the fracture in the ozonosphere has been continuing to increase in recent years, the protection of the skin with the ultraviolet absorber is no longer satisfactory and the necessity for eliminating the active oxygen and free radicals which have been generated as within the cutaneous tissues has been gaining in importance. Further, it has recently come to light that the cytokine, an inflammatory chemical mediator, is derived by an ultraviolet light and that this mediator incites derivation of such immunocytes as leukocytes and consequently gives rise to a local inflammatory reaction and exerts heavy damage on the skin (Thomas S. Kupper etc.: J. Clin. Invest.: Vol. 80, August 1987, 430-436). As the substances that inhibit the manifestation of the cytokine, such steroids as corticosteroid have been known. They are known to possess an effect of repressing immunity and, therefore, incite such harmful side effects as wasting syndrome, diabetes, and osteoporosis. As a result, the desirability of developing a substance which, in the case of a local inflammation of the skin caused by the ultraviolet light, is capable of effectively eliminating the active oxygen and free radicals responsible for the disease and also inhibiting the occurrence of the cytokine which would be otherwise derived has been finding a growing public recognition.
It has further come to light that when the skin is exposed all at once to the stress generated in a large amount as by ultraviolet light, heat, or a chemical substance, this stress entails a decline in the division potential of epicutaneous basal cells and cutaneous fibroblasts besides inducing the local inflammation mentioned above. It is, therefore, inferred that in consequence of this decline of the division potential, the skin as a whole not only succumbs to atrophy but also induces a decrease or alteration in the natural moisture retaining component and the intercellular matrix component produced by the epicutaneous cells and brings about acceleration of cutaneous senescence manifested in the increase of stains and freckles and the formation of wrinkles and curtainings. Thus, attempts have been being made to activate the metabolism of collagen and hyaluronic acid with a view to improving the cutaneous cells in flexibility and resilience and to promote turnover with a view to repressing the deposition of pigment in the skin and promoting the beautification of the skin in white by activating the fibroblasts which synthesize such a matrix component as collagen in the skin. As the substances that activate cutaneous cells and prevent them against senescence, vitamin C, vitamin E, retinoic acid, and retinol derivatives have been known. These substances invariably have a dubious quality in stability, percutaneous absorbency, and teratogenicity and, as such, find utility in an extremely limited range.
The chromanol glycoside which is used in this invention is a known compound (JP-A-07-118, 287, JP-A-09-249,688, and JP-A-11-21,291). The chromanol glycoside is obtained by substituting an alcohol for the phytyl group at the 2 position of the chroman ring of α-tocopherol which is a typical vitamin E and further linking a saccharum to the alcohol. It possesses high solubility in water and excellent resistance to oxidation. It has never been known, however, to utilize the chromanol glycoside mentioned above for the prevention of such cutaneous disorders as described above and as dermatological agent for external uses as curing agents and cosmetic articles.
This invention, initiated in view of the problematic points incurred by the prior art as described above, has as an object thereof the provision of a novel dermatological agent for external use which is capable of effectively acting to repress and cure the dermopathy caused as by the ultraviolet light, for example, at a small application rate without entailing any side effect.
Another object of this invention is to provide a novel dermatological agent for external use which is capable of effectively eliminating the active oxygen and free radicals forming the cause for the local cutaneous inflammation due to the ultraviolet light and, at the same time, repressing the production of a cytokine to be derived therefrom.
A further object of this invention is to provide a novel dermatological agent for external use which is capable of preventing improving the deposition of pigment in the skin by the ultraviolet light and exhibiting an excellent beautification in white.
Still another object of this invention is to provide a novel dermatological agent for external use which is capable of activating the cutaneous cells and preventing the cutaneous senescence.
Yet another object of this invention is to provide a novel dermatological agent for external use which can be obtained as an aqueous preparation containing the active component at a high concentration and which excels instability and percutaneous absorbency.